Transfer of this CIDA to Vanderbilt University is requested to allow collaboration with the sponsor. Dr. Harold Moses. Preliminary data demonstrate an association between cell surface immunophenotype with the karyotype, histopathologic grade of malignant glioma and the duration of clinical survival. It is hypothesized that cell surface antigenic events provide a selective advantage to the expressing neoplasm in association with immunosuppression and/or proliferative stimulation. The mechanism(s) of the latter probably involve growth factors (GF). To further understand the significance of the transformation-related immunophenotypic changes observed, this application proposes to: (1) To determine whether the elements for an autocrine loop exists, the production or absence of the mRNA's and protein products of transforming growth factor-beta (TGF- b1,2,3), transforming growth factor-alpha (TGF-a), epidermal growth factor (EGF), platelet derived growth factor (PDGF), and their respective receptors (where available) will be established among malignant glioma cultures; (2) To correlate the expression of stimulatory GF with clinical, pathologic grade and experimental parameters (the cytogenetic and immunophenotypic abnormalities). Differential expression of GF may provide insights into the sequence of stage-related abnormalities of glioma progression. Additionally, the presence of putatively immunosuppressive TGF-b family gene products will be correlated with the immunophenotypic complexity of the cultures, as well as with the duration of the clinical survival of affected patients; (3) Determine whether a limited number of original biopsies (where available as well as of newly resected primary and recurrent CNS neoplasms (5-10) demonstrate the expression of similar GF/GF- receptor, and immunophenotypic (with a more restricted panel of antigens) correlations EX VIVO as identified IN VITRO. This portion of the investigation will be directed by the findings in 1 and 2. Tumors will be examined by Northern and Southern blot analysis, in situ hybridization and immunocytochemistry for TGF-a/EGF, EGF-R, PDGF, and TGF-b1,2,3.